Volume 903, Issue 1 p. 144-149

Plasma β-Amyloid Peptide, Transforming Growth Factor-β1, and Risk for Cerebral Amyloid Angiopathy

STEVEN M. GREENBERG

Corresponding Author

STEVEN M. GREENBERG

Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA

Address correspondence to Steven M. Greenberg, M.D., Ph.D., Massachusetts General Hospital, Wang ACC 836, Boston, MA 02114, USA. Tel.: (617) 724–1874; fax: (617) 726–5346. e-mail: [email protected]Search for more papers by this author
HYUN-SOON CHO

HYUN-SOON CHO

Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA

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HEATHER C. O'DONNELL

HEATHER C. O'DONNELL

Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA

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JONATHAN ROSAND

JONATHAN ROSAND

Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA

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ALAN Z. SEGAL

ALAN Z. SEGAL

Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA

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LINDA H. YOUNKIN

LINDA H. YOUNKIN

Mayo Clinic, Jacksonville, Florida 32224, USA

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STEVEN G. YOUNKIN

STEVEN G. YOUNKIN

Mayo Clinic, Jacksonville, Florida 32224, USA

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G. WILLIAM REBECK

G. WILLIAM REBECK

Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA

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First published: 30 January 2006
Citations: 23

Abstract

Abstract: Despite the documented association between apolipoprotein E genotype and cerebral amyloid angiopathy (CAA), a substantial proportion of CAA-related hemorrhages occur in patients without known risks for this disorder. Two other factors implicated in the pathogenesis of CAA are the amyloid-β peptide (preferentially deposited in vessels as a 40-amino acid species) and the multifunctional cytokine transforming growth factor-β1 (a specific promoter of vascular amyloid deposition in transgenic models). We measured plasma concentrations of these factors in a series of 25 patients diagnosed with probable or definite CAA-related hemorrhage and compared them with 21 patients with hemorrhage due to probable hypertensive vasculopathy and 42 elderly control subjects without hemorrhage. We found no differences among the groups in concentrations of the 40- or 42-amino acid species of β-amyloid or either the active or latent form of transforming growth factor-β1. While the data do not exclude important roles for these molecules as risks for CAA, they indicate that plasma measurements are not useful in its diagnosis.